Endothelium‐dependent and ‐independent responses to protease‐activated receptor‐2 (PAR‐2) activation in mouse isolated renal arteries

• Published in: British journal of pharmacology 1998-10, Vol.125 (4), p.591-594
• Main Authors: Moffatt, J D, Cocks, T M
• Format: Article
• Language: English
• Subjects: Animals; Biological and medical sciences; Blood vessels and receptors; Endothelium, Vascular - physiology; endothelium‐dependent relaxation; Fundamental and applied biological sciences. Psychology; In Vitro Techniques; Male; Mice; Mice, Inbred BALB C; mouse renal artery; Muscle Contraction - drug effects; Muscle, Smooth, Vascular - drug effects; Nitric Oxide Synthase - antagonists & inhibitors; Oligopeptides - pharmacology; Protease‐activated receptor‐2 (PAR‐2); Receptor, PAR-2; Receptors, Thrombin - metabolism; Renal Artery - drug effects; Special Reports; thrombin receptor; Trypsin - pharmacology; Vertebrates: cardiovascular system
• ISSN: 0007-1188; 1476-5381
• DOI: 10.1038/sj.bjp.0702157

Protease‐activated receptors (PARs) are receptors which require proteolytic cleavage to be self‐activated by newly exposed N‐terminal ‘tethered ligands’, and hence serve as sensors for protelytic enzymes. While both the thrombin receptor (PAR‐1) and PAR‐2 (activated by tryptic enzymes) have been shown to mediate endothelium‐dependent vasorelaxation, only PAR‐1 has been shown to cause direct vascular smooth muscle contraction. In this study, we report that trypsin and the PAR‐2 selective peptide ligand SLIGRL‐NH2 not only caused endothelium‐dependent relaxation of mouse renal arteries but also direct smooth muscle contraction if endothelial nitric oxide synthase was inhibited or if the endothelium was removed. British Journal of Pharmacology (1998) 125, 591–594; doi:10.1038/sj.bjp.0702157